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Histopathology > Histopathology 15 - Cerebrovascular disease and Trauma > Flashcards

Histopathology 15 - Cerebrovascular disease and Trauma Flashcards

1
Q

What are the 2 main types of cerebral oedema?

A

Vasogenic (due to disrupted BBB)
Cytotoxic (due to hypoxia/ ischaemia)

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2
Q

What is the difference between communicating and non-communicating hydrocephalus?

A 
Communicating = problem with CSF resorption into venous sinuses 
Non-communicating = Due to obstruction in flow
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3
Q

What is the normal range for ICP in a supine adult?

A

7-15mmHg

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4
Q

What is the most important contraindication to lumbar puncture?

A

Pailloedema

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5
Q

What is the most common site for non-traumatic intra-parenchymal haemorrhages?

A

Basal ganglia

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6
Q

What is the biggest risk factor for non-traumatic intra-parenchymal haemorrhage?

A

Hypertension

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7
Q

When do congenital arteriovenous malformations tend to become symptomatic?

A

Between 2nd and 5th decade

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8
Q

What is the management of ruptured congenital arteriovenous malformation?

A

Surgically remove if poss, this may be radiosurgery
Embolise (to stop bleeding)

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9
Q

What is a cavernous angioma?

A

Hemangioma (vascular tumour), which causes a slowing of blood flow through “caverns”

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10
Q

When do cavernous angiomas become symptomatic?

A

When they bleed - which is at low pressure and usually >50 years

so essentially after congenital AVMs

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11
Q

What is the most common site of haemorrhage in subarachnoid haemorrhage?

A

Berry aneurysm rupture
80% at internal carotid artery bifurcation

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12
Q

What is the key symptom of subarachnoid haemorrhage?

A

Sudden onset severe ‘thunderclap’ headache

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13
Q

At what size of Berry aneurysm is the risk of rupture greatest?

A

>6mm

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14
Q

How can Berry aneurysms be fixed?

A

Platinum coiling

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15
Q

In which cerebral artery are infarctions most likely?

A

Middle cerebral artery

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16
Q

What % of TBI patients make a good recovery?

A

31%

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17
Q

What are the clinical signs of skull fracture?

A

Otorrhoea and rhinorrhoea with straw-coloured fluid

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18
Q

What is contusion?

A

Brain collision with skull which causes surface bruising

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19
Q

Which structures are mosta affected by traumatic diffuse axonal injury?

A

Midline structures eg corpus callosum

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20
Q

Two types of cerebral infarction

A

Stroke and TIA

TIA is an important predictor of stroke

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21
Q

Commonest vascular territory affected by stroke

A

Middle cerebral artery

22
Q

Vascular territories affected by TIA

A

Can be any

characteristically embolic atherogenic debris from the carotid artery travels to the ophthalmic branch of internal carotid

23
Q

Management of stroke

A

Aspirin +/- dipyridamole

Thrombolytics (if <3h from event)

+/- carotid endarterectomy

Long term: treat HTN, ↓lipids, anticoag

Main imaging: CT-head non-contrast

24
Q

Treatment of TIA

A

Aspirin + dipyridamole
+/- carotid endarterectomy

Long term: treat HTN, ↓lipids, anticoagulants

**same as stroke except for thrombolytics

25
Q

ACA stroke

A

contralateral leg paresis, sensory loss, cognitive deficits (e.g. apathy, confusion, and
poor judgment)

**essentially leg>arm

26
Q

MCA stroke signs

A

contralateral weakness and sensory loss of face and arm
• cortical sensory loss
• may have contralateral homonymous hemianopia or quadrantanopia
• if dominant (usually left) hemisphere: aphasia
• if non-dominant (usually right) hemisphere: neglect
• eye deviation towards the side of the lesion and away from the weak side

**doesn’t affect legs like ACA

27
Q

PCA stroke signs

A

contralateral hemianopia or quadrantanopia • midbrain findings: CN III and IV palsy/pupillary changes, hemiparesis • thalamic findings: sensory loss, amnesia, decreased level of consciousness • if bilateral: cortical blindness or prosopagnosia • hemiballismus

28
Q

Basilar artery stroke signs

A
  1. Proximal (usually thrombosis): impaired EOM, vertical nystagmus, reactive miosis, hemi- or quadriplegia, dysarthria, locked-in syndrome, coma
  2. Distal (usually embolic, i.e. top of the basilar sydrome): somnolence, memory and
    behavior abnormalities, oculomotor deficit
29
Q

PICA signs

A

PICA (lateral medullary or Wallenberg syndrome): ipsilateral ataxia, ipsilateral Horner’s, ipsilateral facial sensory loss, contralateral limb impairment of pain and temperature
sensation, nystagmus, vertigo, nausea/vomiting, dysphagia, dysarthria, hiccups

30
Q

Lacunar infarct: where is this?

A

(deep hemispheric white matter; involving deep penetrating arteries of
MCA, circle of Willis, basilar, and vertebral arteries)

  1. Pure motor hemiparesis (posterior limb of internal capsule): contralateral arm, leg,
    and face
  2. Pure sensory loss (ventral thalamic): hemisensory loss 3. Ataxic hemiparesis (ventral pons or internal capsule): ipsilateral ataxia and leg
    paresis 4. Dysarthria-clumsy hand syndrome (ventral pons or genu of internal capsule):
    dysarthria, facial weakness, dysphagia, mild hand weakness and clumsiness
31
Q
A
32
Q

Types of non-traumatic haemorrhage

A

Intraparnehchymal

Subarachnoid

33
Q

Most common cause of intraparenchymal haemorrhage

A

50% due to HTN

34
Q

Common site of intraparenchymal haemorrhage

A

Basal ganglia

35
Q

Most common cause of subarachnoid haemorrhage

A

85% of ruptured berry aneurysms

36
Q

Most common location of SAH

A

Internal carotid artery bifurcation

37
Q

What causes charcot-bouchard microaneurysms

A

Non-tramautic intraparnechymal haemorrhage

38
Q

RF of SAH

A

F>M, usually <50yrs, → thunderclap headache, vomiting and LoC, ↑in PKD, Ehler’s Danlos and Pts with Aortic Coarctation. Also associated with vascular abnormalities incl AV malformations, capillary telangiectasias, venous and cavernous angiomas, Ehlers Danlos.

39
Q

Types of traumatic haemorrhage

A

Extradural

Subdural

Traumatic parenchymal injury

40
Q

Extradural haemorrhage

A

Skull fracture, ruptured middle meningeal artery → rapid arterial bleed, lucid interval then LoC,

41
Q

Which type of haemorrhage give syou lucid interval?

A

Extradural haemorrhage

42
Q

Subdural haemorrhage

A

Prev history of minor trauma → damaged bridging veins with slow venous bleed, often elderly/alcoholic, associated with brain atrophy, fluctuating consciousness

43
Q

Types of traumatic parenchymal injury

A

Concussion: Transient LoC and paralysis, recovery in hours or days

● Diffuse axonal injury: Vegetative state, post traumatic dementia

● Contusions: When brain contacts skull +/- fracture.
● Traumatic intracerebral haemorrhage

44
Q

Coup vs contracoup

A

Coup - where the impact occurs

Contracoup - opposite to region impact

45
Q

Causes of increased ICP

A

: Caused by oedema, space occupying lesion (e.g. tumour, abscess) or both → brain herniation.

46
Q

Six types of brain herniation

A

Uncal, Central (transtentorial), Cingulate (subfalcine), Transcalvarial, Upward, Tonsillar.

47
Q

Causes ofbacterial meningitis by age

A

Neonatal to 3 months: Group B streptococcus (GBS) early (90% day 1–5) or late (10% 6 days–3 months), E. coli, Listeria monocytogenes.

• 1 month to 6 years: Neisseria meningitidis (meningococcus), Streptococcus pneumoniae,Haemophilus influenzae type B (Hib).

• >6 years: N. meningitidis (14–25 years), Strep. pneumoniae, mumps (pre-MMR).

• Mycobacterium tuberculosis: Can cause TB meningitis at all ages. Most common in children 6 months–6 years.

• Older adults: Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus
influenzae type b (Hib), group B Streptococcus, Listeria monocytogenes

48
Q

Viral causes of meningitis

A

Enteroviruses (80%), cytomegalovirus (CMV), arbovirus. Herpes simplex virus (HSV) is more likely to cause encephalitis

  1. Herpes simplex most common in adults. All others most common in children and
    infants.
49
Q

meningitis LP finidngs

A
50
Q
A
51
Q

Which lobe of the brain is affected by HSV encephalitis?

A

Temporal lobe

Histopathology (18 decks)

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